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Monday, August 25, 2014

The prevalence of clinical depression is about one third
higher among obese versus non-obese subjects and there is conflicting evidence
as to whether it is depression that brings on obesity or the reverse, where
obesity brings on depression. To study this conundrum, a recent research
project examined data from a longitudinal study of 18, 558 British individuals
born in 1958[1].
This cohort was followed up at 7, 11, 16, 23, 33, 42, 45 and 50 years. Subjects
were rated as underweight, normal weight over weight or obese. Those that were
underweight had 1.3 to 2.3 times the risk of being depressed compared to those
of normal weight. There was no evidence of a tendency toward depression among
the overweight but among the obese, the risks of depression were between 1.5
and 2.3 times that of normal weight subjects. The data were then examined to
see how either one of the conditions (obesity or depression), in prior years
influenced the likelihood of the other condition subsequently developing. Being
underweight predicted subsequent depression in both males and females (25%
higher that those of normal weight) and depression predicted subsequent
underweight in males only(84% higher
risk). Obesity predicted subsequent depression in females only (34% higher
risk). However, depression did not predict subsequent obesity. In all these
calculations, confounding factors such as social class, physical illness and
ethnicity were controlled for.The
authors reflect on the fact that the treatment of obesity should also include
an examination of possible depression but they ignore the elephant in the room,
which is the stigmatization of the obese. By and large, the overweight and
obese are seen by society, including health professionals, as having themselves
to blame. They are seen as lazy, dishonest, untidy, lethargic, unreliable and
so on. Sympathy with the overweight and obese is a rare occurrence.

A second paper[2]
looking at a related topic, namely phobic anxiety, obesity and genes is also
worth considering. Phobic anxieties relate to a wide range of fears that some
people experience and the level of anxiety is measured on the Crown Crisp Index,
which includes, for example, measures of claustrophobia fear of heights and crowds
or hypochondriac traits. The subjects were participants in the Harvard based
Nurses Health Study (5,911 females) or the Health Professional follow-up Study
(3,697 males). They used genetic data on 34 genes linked to obesity. One was
the FTO gene, which is the most widely studied such gene and another was the
gene for a brain receptor involved in appetite regulation (MC4R). The remaining
32 genetic variants had been previously identified as increasing the risk of
obesity in another study and were termed obesity risk genes. One of these 32 genes
was also the FTO gene and these 32 genes had an additive effect on the risk of obesity.
Average phobic anxiety scores were more 43% higher in women, which agrees with
the general literature. The relationship between genetic factors and BMI was
strong for the FTO gene, the MC4R gene and the 32 obesity risk genes. Higher
BMI values increased the risk of phobic anxiety only among those carrying the
common FTO genetic variant. After adjusting to an average BMI value, the FTO
gene variant still had a direct association with phobic anxiety. Taken
together, these data show that there is a common genetic link between obesity
and phobic anxiety. The authors ask that their findings should be treated with
caution and their hypothesis should be studied in larger samples. The finding
that the collection of genes that had a linear rise in the risk of obesity did
not link with anxiety suggests that obesity per se is not a cause of phobic
anxiety and that the two conditions, obesity and phobic anxiety simply share a
common genetic pathway

All in all, these two papers highlight the need for the study
of the psychological conditions associated with obesity and they further
highlight the need to study the reverse: how do psychological conditions
contribute to energy imbalance

Thursday, August 21, 2014

In the 1990’s, antioxidants were the big fashion in food and
health. These antioxidants were mainly vitamins (C and E), pre-vitamins
(beta-carotene) and plant constituents of various kinds (e.g. coumarin,
flavonoids, thymol). Studies showed that rates of cancers across many countries
were directly correlated with plasma levels of antioxidants. Laboratory studies
showed that the damaging effect of pro-oxidant metals such as copper could be
reduced with the addition of antioxidants. Every disease imaginable was
included in the antioxidant Klondike. And of course we had the race to the
finish culminating in a trial of Chinese smokers (smoking is pro-oxidant) with
antioxidant supplements which showed the opposite to what was hoped for - cancer
rates were increased! Many other trials were conducted but to date, little
evidence exists to support the theory that taking antioxidant supplements
reduces any disease risk. Of course that doesn’t bother the health food
industry and to some extent the food industry from hyping up the antioxidant
myth.This blogger learned one lesson
from the antioxidant saga namely that any nutritional theory that is putatively
related to many diseases, is a theory about to be shelved.

In today’s world of food and health, that role is played by
the human gut microbiota. The front covers of The Economist, the New York Times
magazine, Nature, Scientific American and others have highlighted articles with
titles such as “Microbes maketh man” or “Our other genome”. There are wow
statistics that journalists love: 100 trillion bacteria in our gut accounting
for 1.5 kg of our bodyweight with 100 times more genes than we have (“We” are
referred to as “Hosts”!). To journalists, it is an astonishing mystery that
bacteria, previously thought to be bad for health were in fact our single most
important protection against an array of diseases. A search of the PubMed database shows the term
“Gut microbiome” is associated with the following diseases (number of published
papers in brackets): obesity (628), cancer (381), diabetes (350), allergy
(260), depression (48) and autism (33). I stopped there but I’m sure I could go
further. The point is that the gut microbiota is the new unifying theory of
life and death.

A very welcome paper in this week’s Nature bears the title
“Microbiome science needs a healthy dose of sceptism”[1].
The author’s first point of criticism is that the techniques used to
characterise the microbiota genome often lack direct links to known functions.
He points out that his team has shown that vaccination eliminated 30% of known
pneumococcal strains in a human population but only because they knew which
genes to focus on. In the case of the human microbiota genome, we might know
that it differs between say normal weight and obese subjects. But that’s all we
know. We cannot tell what part of the microbiota genome is directly linked in a
causal manner to obesity.His second
criticism is linked to this in that cause and effect are misinterpreted when
looking at gut microbiota. He cites a paper, which shows that changes in the
human microbiota correlate with measures of frailty in older persons. So too
did dietary patterns. The conclusion was that poor diet altered the gut
microbiota and thus led to frailty. The opposite was not considered, namely,
that frailty led to poor diets that in turn altered gut microbiome patterns.
His third criticism is that most of the studies lack any mechanistic
explanation based on experimental investigation. In that respect the field is
similar to nutritional epidemiology where correlations dominate and shape
policy in the absence of any experimental proof. So if we consider the
microbiome-diet-frailty issue, a simple test would be to take a cohort of frail
persons and through physiotherapy, counseling and nutritional support reduce
their frailty. If a significant improvement in frailty had no effect on the
microbiome, we can dismiss that theory. Alternatively, frail persons could
receive faecal transplants to modify their microbiota and examine the effect of
improved microbiota on frailty. His fourth criticism relates to the quality of
the data on the microbiota and health vis-à-vis the real world. He highlights
the fact that many of the studies that show the importance of the gut
microbiota are conducted in germ-free mice. Such mice live in an aseptic bubble
that makes them generally ill and with poor food intake. Finally he asks if
there might be a confounding factor such that the real force driving the
disease is one thing and the altered microbiota simply an observer, equally
effected by the true driver.

In his paper, Professor Hanage who works in Harvard, cites a
blog by Professor Jonathan Eisen of the University of California at Davis in
which he makes an award for “Overselling the microbiome”[2].
He shows how research results are manipulated by university press offices and
swallowed easily by journalists. Two collaborating Swedish university research
groups published a paper in Nature Communications[3]
and they wrote thus:

“Our finding of
enriched levels of phytoene dehydrogenase in the metagenomes of healthy
controls and its association with elevated levels of β-carotene in the serum may
indicate that the possible production of this
anti-oxidant by the gut microbiota may have a positive health
benefit”.

“Our results indicate
that long-term exposure to carotenoids, through production by the bacteria in
the digestive system, has important health benefits. These results should make
it possible to develop new probiotics. We think that the bacterial species in
the probiotics would establish themselves as a permanent culture in the gut and
have a long-term effect”. “By examining the patient's bacterial microbiota, we
should also be able to develop risk prognoses for cardiovascular disease",
says Fredrik Bäckhed, Professor of Molecular Medicine at Gothenburg University.
"It should be possible to provide completely new disease-prevention
options".

The present fashion of the microbiota has a powerful
scientific dimension but it is over-hyped and under-studied at the human
experimental level. Whist many good human experiments are done to study the
human microbiota, most are poorly constructed, observational and in rodents,
normal or germ free.

Saturday, August 2, 2014

Maureen Ogle, in her book “In meat we trust”, reminds us that
school lunches have always been on the menu of food controversies. In 1926, the
New York School Board banned frankfurters from school lunches. She writes that:
“The board’s lunch director explained that the food was unsuited to students’
nutritional needs” The director went on to say that: “The sausage was so heavy
that when children ate it, they neglected to eat green stuff and milk”. And
you’ve guessed it – no data were gathered upon which to construct evidence
based policy. The director simply looked into his or her heart in search of
wisdom. The issue of school lunches lingers on and whilst I want to end on a
positive note, I will cite three studies which all show that poorly informed or
misinformed interventions in food choice to improve nutritional balance in
school lunches can back fire.

Case 1. A group
from Tufts University examined the effect of three years of intervention in the
US National School Lunch Programme to reduce total fat and saturated fat intake[1].
They observed that as the % of calories in lunches decreased, the % of calories
from fat increased. This is known as the sugar-fat seesaw. Basically, if one
reduces the level of fat in a child’s energy supply, children will compensate
for the loss of fat by eating higher amounts of other foods and time after
time, it has been shown that as you lower fat, you raise sugar. So, in today’s
terms where sugar is popularly perceived to be utterly toxic, would one
describe the reduction in total fat and saturated fat intakes as a success or
would the increase in % energy from sugars be seen as a failure. This writer
would deem it a success as fats and especially saturates are directly
implicated in elevated plasma cholesterol on the basis of dozens of randomised
controlled feeing studies while almost none exist for sugar at the normal or
even slightly normal levels of intake.

Case 2. Fruit and
vegetable intake are common targets in school lunch programmes and the general
belief is that because they have a low energy density (fewer calories per unit
weight) that higher intakes will reduce energy intake. Researchers from the
University of Wiscanson-Maddison studied food choice in school canteens using
digital imaging to identify foods selected and portion size[2].
They studied schools taking part in the Farm to School project. They found that
whereas fruit and vegetable intake increased, the intake of other foods
decreased such that energy intake remained constant. Thus if the objective was
to reduce energy intake, the project failed. But a higher intake of low-salt,
low fat fruit and vegetables would reduce overall the negative targets of foods
(fats, saturates etc.) and thus the project should be deemed a success.

Case 3: Brian
Wansink and his colleagues at Cornell University, reported on a pilot study
evaluating the consequences of banning chocolate milk in school cafeterias[3].
Chocolate flavoured milk represents about two thirds of all mile in the US
school cafeteria system. In 11 Oregon schools, chocolate flavoured milk was
banned from the lunch menu and the group from Cornell used data gathered in the
National School Lunch Program to assess the success or otherwise. Total milk
sales fell by 10%. White milk increased but some 29% of this non-flavoured milk
was wasted, that is unfinished by the students. In all, the numbers of children
using the School Lunch Program fell by 7%. Success or failure? Once again I
would say the outcome could have been predicted if someone had invested funds
in attitudinal research, which would have saved a lot of money and effort.My father, a carpenter, always used the phrase: “Measure twice – cut once”. In effect, these school lunch managers, in all three cases never measured even once. But they were all mad keen to cut!

Which brings us to a major recent study from the University
of Chicago, which carried out a survey of 557 representative schools to assess
the impact of the updated standards of the National School Lunch Program[4].
The ratio of “agree”/ “agree strongly” to “disagree”/ “disagree strongly” that
“students generally seem to like the new school lunch” was about 70:30. This
contrasts with the opinion: “At first, students complained about the new lunch”
where 57% agreed or agreed strongly. So, slowly the students absorbed the newer
healthier lunches. About 2/3 students have fewer complaints about the new
lunches and the same number doesn’t seem concerned about the changes. One main
area of complaint was the withdrawal of pizzas from some school menus. Students
were happy with healthier pizzas but not happy with the absence of any pizza
option. So this is a positive note for innovation school lunches. However, the
more that innovation is built on a priori
data, the more likely it is to be successful and, regrettably, the general
trend is to cut and not measure in advance.

Here in the EU, where national policies on school lunches
differ according to member state, the Commission has published a very useful
overview of existing practices and has set the scene for future joint action to
help improve the nutritional quality of school lunches[5].

One area of public health nutrition that is badly missing is
the measure of the impact of school lunches on the student’s overall daily
dietary performance. In other words, for how many children does the school
lunch counter balance poor dietary practices at home and outside the home and
school environments? For how many pupils is the home driving most the student’s
daily intake of nutrients to optimal. Such data are very important to
understand the true social impact of school lunches.

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"Ever seen a fat fox ~ Human obesity explored"

About Me

I graduated from University College Dublin in 1971 with an Masters in Agricultural Chemistry, took a PhD at Sydney University in 1976 and joined the University of Southampton Medical School as a lecturer in human nutrition in 1977. In 1984 I returned to Ireland to take up a post at the Department of Clinical Medicine Trinity College Dublin and was appointed as professor of human nutrition. In 2006 I left Trinity and moved to University College Dublin as Director of the UCD Institute of Food and Health. I am a former President of the Nutrition Society and I've served on several EU and UN committees on nutrition and Health. I have published over 350+ peer reviewed scientific papers in Public Health Nutrition and Molecular Nutrition and am principal investigator on several national and EU projects (www.ucd.ie/jingo; www.food4me.org). My popular books are "Something to chew on ~ challenging controversies in human nutrition" and "Ever seen a fat fox: human obesity explored"